Cerebral palsy is defined as a non -progressive neuromotor disorder of cerebral orgin
1. Maldevelopment and disorderly anatomic organisation of brain
2. Perinatal hypoxia
3. Birth trauma
4. Acid base imbalance
5. Indirect hyperbilirubenamia
6. Metabolic disturbance
7. Intra uterine or acquired infection
Pathological lesion such as cerebral atrophy porencephaly leucomalacia. Degeneration of basal ganglia cerebelar lesion
A) SPASTIC CEREBRAL PALSYDepending upon distribution of spasticity
it may be
1. Spastic quadriplegia
it is more commen in term baby . Ht include opisthotonos posture ,pseudobulbar palsy ,feeding difficulties ,restricted voluntary movements. And multiple deficits .
2SPASTIC DIPLEGIAcommoner in preterm babies and associated with periventricular leukomalacia . the lower limbs are more severily affected with extension and adduction posturing. Brisk tendon jerks and tendency to contracture .
3.SPASTIC HEMIPLEGIARecognition after 4 to 6 months age due to poor observation
Abnormal persisting fisting., abnormal posture or gait disturbance,vascular insult , porencephaly or cerebral anomalies may be associated
B) HYPOTONIC CEREBRAL PALSYDespite pyramidal involvement there patient are atonic or hypotonic .
tendon reflexes are normal or brisk and Babinski personse is positive .
They are often severely mentally retarded .
In cerebral involvement hypotonic is not associated with exaggerated reflexes .
C) EXTRAPYRAMIDAL CPThe clinical features include dyskinesia such as athetosis , choriform movements , dystonia tremors and rigidity
Arms legs trunks may be involved
mental retardation and hearing defect may be present .
Cerebral damage following bilirubin encephalopathy is a classical example and deafness is commonly associated.
In cerebral involvement there is hypotonia and hyporeflexia.
Ataxia and intentional tremors appear by the age of 2yrs.
ASSOCIATED FEATURES1. EYES
Strabismus, Paralysis of gaze,
cataract,colobama, refractive errors.
2. Ear :) loss of hearing
3. speech aphasia ,dysarthria and dyslalia
4. Sensory defects asereogenosis and spatial disorientation are seen.
5. generalised or focal seizures
6. Mental retardation
DIAGNOSIS1. Suspected in following cases
low birth weight ,perinatal insult has increased tone ,feeding difficulties and does not keep pace with anticipited normal range of neurological and behavioural development .
2. evaluation of patient include perinatal history ,detailed neurological and developmental examination , electroencephalogram,psychometric and sensory evaluation .
3. assessement of learning and language difficulties .
4. aminoaciduria should be exclude by chromatography of urine and plasma
PREVENTIONcan be prevented by prevention of infection ,fetal of perinatal insult ,hmmm maternal care and freedom from postnatal damage reduce prevalance .
1. SYMPTOMATIC treatment for seizuries.
2. Tranquilizers are administered for behaviour disturbances .
3. Muscle relaxants for improving muscle function
4. Baclofen helps to reduce spasticity ,
Dantrolene sodium for relaxation of skeleton muscle .local phenol block .
OCCUPATIONAL THERAPYsimple movements of self help with progressive development of more intricate activities .
EDUCATIONALTHE Defect of vision ,speech, and learning are managed by adequate
ORTHOPEDIC SUPPORT by light wt splint
SOCIAL SUPPORT TO FAMILY
REHABILITATION AND VOCATIONIBL GUIDANCE